Implantable stimulation devices or cardiac pacemakers are a class of cardiac rhythm management devices that provide electrical stimulation in the form of pacing pulses to selected chambers of the heart. As the term is used herein, a pacemaker is any cardiac rhythm management device with a pacing functionality regardless of any additional functions it may perform, such as cardioversion/defibrillation.
A pacemaker is comprised of two major components, a pulse generator and a lead. The pulse generator generates the pacing stimulation pulses and includes the electronic circuitry and the power cell or battery. The lead, or leads, is implanted within the heart and has electrodes which electrically couples the pacemaker to the desired heart chamber(s). A lead may provide both unipolar and bipolar pacing and/or sensing configurations. In the unipolar configuration, the pacing pulses are generally applied (or responses are sensed) between an electrode carried by the lead and a case of the pulse generator or an electrode of another lead within the heart. In the bipolar configuration, the pacing pulses are applied (or responses are sensed) between a pair of electrodes carried by the same lead.
When the patient's own intrinsic rhythm fails, pacemakers can deliver pacing pulses to a heart chamber to induce a depolarization of that chamber, which is followed by a mechanical contraction of that chamber. For example, the pacemaker may deliver bi-ventricular (BiV) pacing pulses to the left ventricle (LV) and right ventricle (RV) of the heart. Conventionally, BiV pacing occurs at an expiration of a fixed atrio-ventricular (AV) delay that preempts a patient's intrinsic cardiac conduction to force BiV pacing therapy. Pacemakers further include sensing circuits that sense cardiac activity for the detection of intrinsic cardiac events such as intrinsic atrial depolarizations (detectable as P waves) and intrinsic ventricular depolarizations (detectable as R waves). By monitoring cardiac activity, the pacemaker circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pacing pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle when required to help stabilize the electrical rhythm of the heart. This therapy is referred to as cardiac resynchronization therapy (CRT).
However, some patients fail to respond to conventional CRT. Existing BiV pacing techniques do not adapt to changes in patient status. Thus, it becomes important to take into account changes in a patient's intrinsic conduction time, which can affect appropriate timing of the BiV pacing pulses. For example, the intrinsic conduction time of the patient can change in response to variations in heart rate, activity level (e.g., exercise), medications, clinical status, and/or the like. Additionally, existing BiV pacing techniques are not customizable to patient-specific timing.
Patients with wide QRS duration and left bundle branch block (LBBB) typically derive the most benefit from CRT. In addition, targeting the site of latest LV electrical activation with BiV pacing has been shown to be associated with reverse ventricular remodeling and quality of life improvements. These studies implicate that LV electrical dyssynchrony plays an important role in CRT response and taken together suggest a role for correction of electrical dyssynchrony in improving response to CRT using BiV fusion pacing. BiV fusion pacing corresponds to timing the BiV pacing pulse to arrive coincident with a patient's intrinsic right bundle conduction.
While BiV fusion pacing has proven to be beneficial in certain patients, there is still room for improving BiV pacing techniques to further improve patient outcomes.